Your hidden mind defenses against Alzheimer’s
It has been recognized for some time that Alzheimer’s disease affects the areas of the brain in a different way and that Tau – a protein known for misconduct – plays an important role in the disease. Usually, Tau helps stabilize nerve cells, but in Alzheimer’s disease, it begins to make mistakes and tangle inside neurons. It spreads through the brain to form toxic groups that weaken the function of neurons and ultimately leads to cell death.
The brain areas such as the inner cortex and the horses early surrender to Tanguko Tau, while other areas, such as primary sensory cortical, remain flexible to the disease. In seeking to better understand this selective weakness (SV) or flexibility (SR) of Alzheimer’s disease, the researchers looked at the genetically modified genes and studies to determine the genes of Alzheimer’s risk. But the previous research did not show a clear link between the location of genetic risk factors and its associated Tau.
Now, a new study conducted by the University of California in San Francisco jumped towards answering this question – by combining brain imaging, genetics, and advanced sporty modeling into a strong new lens. The study, published on July 9 in brainIt appears multiple distinctive paths that give risk genes through weakness or flexibility in Alzheimer’s disease.
The study presented a model for the spread of the disease called the EndM network. The researchers applied this model on brain tests from 196 individuals at different stages of Alzheimer’s. They put forward what the model predicted from what they saw in the examination operations. Food residue, called “remaining Tau”, pointed to the areas where something else affects the brain’s contacts on the accumulation of Tau – in this case, genes.
Using the maps of the genes of the brain from the atlas of the human brain Allen, researchers tested the degree in which the genes of the risk of Alzheimer’s are explained by the actual and remaining tau. This allowed them to dismantle the genetic effects that work with or independent of the brain wire.
“We think about our model as the Google Maps of Tau,” said Ashish Raj, a doctorate, a professor of x -ray and biomedical photography. “It predicts the place where the protein will go after that, using the real world’s brain contact data from healthy people.”
This raises the traditional view of how Tao moves in the brain
The study team has revealed four types of genes that are distinguished based on the amount of pace of Tao: the vulnerability to the network (SV-NA), which are genes that enhance Tao along the brain wire; SV-Ni, which are genes that enhance Tau in unrelated ways to connect; The flexibility of the network (SR-NA), which are genes that help protect the areas that are otherwise the hot points Tau; The flexibility is independent of the network (SR-NI), which are genes that provide protection outside the usual path of the network-such as hidden shields in unbearable spots.
The first author in the study, Chitali Anand, a post-PhD researcher at UCSF: “The alignment genes participated in weakness with stress, metabolism and cell death; genes associated with flexibility participated in the immune response and the cleaning of the Beta-one of the perpetrators is another for Alzheimer’s.” “On its essence, genes that make parts of the brain or less affected by Bazheimer work through different functions – some control how Tao moves, while others deal with internal defenses or cleaning systems.”
This research based on another recent Ucsf study in mice, published May 21 in Alzheimer’s and dementiaWhich showed that Tao does not travel randomly or spread negatively; Instead, it follows the paths of wires in the brain with a distinctive directional preference. Using a system of differential equations called the NDM model (NDM), the research team enables the Tau spread dynamics between the connected brain areas, which challenges the traditional view that Tao is simply spreading by spreading across space outside the cell or leakage of deadly neurons.
“Our research has shown that Tao is spreading simultaneously, as he travels along the central projections driven by active transportation instead of negative spread, and the exploitation of active nerve paths in the favorite reactionary direction,” said Justin Torok, a post -PhD researcher who works in the Raj Laboratory.
In the current study, the network -based analyzes have completed the current methods to verify the authenticity and identification of genes based on weakness and selective flexibility. Genes that respond independently from the network have biological functions different from those genes that respond in coordination with the network.
“This study provides an optimistic map forward: one mixes biology and brain maps in a more intelligent strategy to understand Alzheimer’s disease and ultimately stopped,” said Raj. “The results we have reached are new visions in the signature signatures in Alzheimer’s disease and may be useful in determining the potential intervention goals.”
Another additional: Make Abdur, Benjamin Sebes, Darren Maya, PhD.
Funding: The search was partially supported by Nih Grants R01NS092802, RF1AG062196 and R01ag072753 granted to Ashish Raj.
(Tagstotranslate) nervous system; Healthy aging, immune system; Alzheimer & amp;#039; S; Difference; Alzheimer’s & amp;#039; S; Neuroscience
Post Comment